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D'Angelo, D.* ; Vecellio Reane, D. ; Raffaello, A.*

Neither too much nor too little: Mitochondrial calcium concentration as a balance between physiological and pathological conditions.

Front. Mol. Biosci. 10:1336416 (2023)
Verlagsversion DOI PMC
Creative Commons Lizenzvertrag
Ca2+ ions serve as pleiotropic second messengers in the cell, regulating several cellular processes. Mitochondria play a fundamental role in Ca2+ homeostasis since mitochondrial Ca2+ (mitCa2+) is a key regulator of oxidative metabolism and cell death. MitCa2+ uptake is mediated by the mitochondrial Ca2+ uniporter complex (MCUc) localized in the inner mitochondrial membrane (IMM). MitCa2+ uptake stimulates the activity of three key enzymes of the Krebs cycle, thereby modulating ATP production and promoting oxidative metabolism. As Paracelsus stated, "Dosis sola facit venenum,"in pathological conditions, mitCa2+ overload triggers the opening of the mitochondrial permeability transition pore (mPTP), enabling the release of apoptotic factors and ultimately leading to cell death. Excessive mitCa2+ accumulation is also associated with a pathological increase of reactive oxygen species (ROS). In this article, we review the precise regulation and the effectors of mitCa2+ in physiopathological processes.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Calcium ; Cell Death ; Metabolism ; Mitochondria ; Mitochondrial Calcium Uniporter (mcu); Inositol 1,4,5-trisphosphate Receptors; Pyruvate-dehydrogenase Phosphatase; Linked Isocitrate Dehydrogenase; Endoplasmic-reticulum Ca2+; 2-oxoglutarate Dehydrogenase; Signal Transmission; Adenine-nucleotides; Essential Component; Ca-2+ Ions; Rat-heart
Sprache englisch
Veröffentlichungsjahr 2023
HGF-Berichtsjahr 2023
ISSN (print) / ISBN 2296-889X
e-ISSN 2296-889X
Quellenangaben Band: 10, Heft: , Seiten: , Artikelnummer: 1336416 Supplement: ,
Verlag Frontiers
Verlagsort Lausanne
Begutachtungsstatus Peer reviewed
POF Topic(s) 30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502295-001
Förderungen European Union
European Union (Next-Generation EU)
Italian Ministry of University and Research
Scopus ID 85180687365
PubMed ID 38148906
Erfassungsdatum 2024-01-09